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Research and educational purposes only. This library summarises published research and regulatory status. It is not medical advice, not a recommendation to use any compound, and not a substitute for a licensed professional. Intended for adults.

Library

SLU-PP-332

Pan-ERR agonist (small molecule, not a peptide)

Also known as: Slu pp 332, Pan-ERR agonist SLU-PP-332

Evidence level: Early/animal research

What it is

SLU-PP-332 is studied as an 'exercise mimetic': researchers are interested in it for reproducing training-like effects such as more oxidative muscle fibers, better endurance, and reduced fat mass in animal studies, by activating a group of receptors called ERRs. It's a small molecule, not a peptide, included here because it's used alongside peptide protocols; the lab that created it found it doesn't absorb well when swallowed, so animal studies injected it even though it's sold as an oral product. It is not FDA-approved and has no completed human clinical trials — the evidence is exclusively preclinical, and it's sold only as a research compound.

What the research found

SLU-PP-332 has been studied as an "exercise mimetic" (an ERR agonist), and the evidence is exclusively preclinical. In mice it has been reported to increase oxidative muscle fibers, enhance exercise endurance, and reduce fat mass in obese animals. No human pharmacokinetic or clinical study exists, and the human dose range is not established.

Status and regulatory position

Not FDA approved for any indication. Preclinical research compound — ClinicalTrials.gov returned zero registered SLU-PP-332 trials as of 2026-07-18.[¹] Available in research-community contexts as a research compound. Not a peptide — SLU-PP-332 is a small-molecule synthetic compound; it is included in the Vialwise library because the library scope explicitly extends to "compounds researchers running peptide protocols use" rather than peptides only. WADA: not named in the 2026 Prohibited List, but captured by S0 by default and high-risk besides. Two WADA-accredited laboratories published detection assays in 2026 describing SLU-PP-332 as having doping potential in the metabolic-modulator class. Do not assume it is permitted; researchers competing in WADA-tested sport should confirm against the most recent edition and with their anti-doping organization before any competitive event.

Safety

SLU-PP-332 is not FDA-approved and has no human clinical trial data, so its safety and off-target effects in people are not characterized. It is not named on the WADA Prohibited List, but it has no approval as a medicine anywhere, and WADA's S0 category prohibits exactly that by default. Two WADA-accredited labs have also published detection methods for it and describe it as having doping potential — anyone in tested sport should treat it as off-limits and check with their anti-doping organization. VialWise is a research and educational reference, not medical advice — consult a licensed professional.

Disclosures

⚠️ For research and educational purposes only. SLU-PP-332 is not approved by the FDA or any major Western regulatory agency as a pharmaceutical drug for any indication. Information in this entry is informational, not medical advice. Always confirm dose calculations and consult appropriate professional guidance before any protocol decisions.

⚠️ not a peptide — small-molecule synthetic compound. SLU-PP-332 is a small-molecule pan-agonist of the estrogen-related receptors (ERRα, ERRβ, ERRγ), structurally and pharmacologically distinct from the peptide compounds that comprise most of the Vialwise library. The compound is included in the library because the library scope explicitly broadened to "compounds researchers running peptide protocols use" — researchers using SLU-PP-332 are typically also using peptides in stack protocols, and the Vialwise framing of dose, regulatory status, and safety considerations applies. The reconstitution and calculator framework that applies to peptide compounds does not apply to SLU-PP-332 — it is supplied as a small-molecule preparation, not reconstituted from lyophilized powder. Note that the research-chemical market supplies it in oral formats even though the originating lab reports the compound lacks oral bioavailability.[⁴]

⚠️ Preclinical research compound — no completed human clinical trials. As of this entry's last-updated date, no registered or completed Phase 1/Phase 2/Phase 3 clinical trial for SLU-PP-332 exists on ClinicalTrials.gov. The compound's evidence base is exclusively preclinical (cell culture, mouse models). The dose ranges used in research-community human protocols are extrapolated from animal model studies plus accumulated researcher experience — they should be presented to users as observational, not validated. Researchers should be explicit with themselves about the genuinely-only-preclinical evidence base when interpreting any subjective effects of human use.

⚠️ Mechanism — pan-agonism of estrogen-related receptors (ERRα/β/γ). SLU-PP-332 is a synthetic small-molecule pan-agonist of the estrogen-related receptor family — three orphan nuclear receptors (ERRα, ERRβ, ERRγ) that sit upstream of mitochondrial biogenesis, fatty acid oxidation, and the aerobic gene program activated by endurance exercise.[¹] The compound has the highest potency for ERRα. Activation of the ERR pathway in skeletal muscle cell lines increases mitochondrial function and cellular respiration; in mice, SLU-PP-332 increases type IIa oxidative skeletal muscle fibers, enhances exercise endurance, and produces metabolic effects mimicking aerobic exercise (increased energy expenditure, fatty acid oxidation, improved glucose tolerance, reduced fat mass in obese animals).[¹] The "exercise mimetic" framing is mechanistic — SLU-PP-332 activates many of the same intracellular pathways exercise activates, but does not substitute for the broader physiological adaptations exercise produces.

⚠️ Pan-ERR agonism affects multiple tissues; off-target effects are not fully characterized. ERRα, ERRβ, and ERRγ are expressed across multiple tissues (skeletal muscle, heart, liver, brain, kidney, reproductive tissues) with distinct tissue-specific transcriptional roles. Pan-agonism (activation of all three receptors) can produce desired metabolic effects but also potential off-target effects in non-skeletal-muscle tissues. The full off-target profile in humans is not characterized given the lack of clinical trial data. Researchers should not infer that SLU-PP-332's "exercise mimetic" effects are selective to skeletal muscle metabolism.

Quick reference

Compound classSmall-molecule synthetic compound; pan-agonist of estrogen-related receptors α, β, γ. Not a peptide.
Common formulationsOral powder or capsules from research-chemical suppliers. No FDA-approved or pharmaceutical-grade product exists.
FrequencyDaily during research-community use, often with food
Half-lifePlasma half-life in humans is not characterized — no published human pharmacokinetic study exists. ⚠️ Oral bioavailability is not supported: the originating Burris lab states that SLU-PP-332 "lacks oral bioavailability," which is the stated reason they developed the successor compound SLU-PP-915.[⁴]
Route⚠️ Route claims here are contested. Research-chemical vendors sell SLU-PP-332 as an oral preparation and research-community use is predominantly oral — but that is a market observation, not a pharmacokinetic finding. In the published mouse studies the compound was dosed intraperitoneally, and the originating lab reports it lacks oral bioavailability.[⁴] Some research-community materials reference subcutaneous use. No route has validated human PK data.
Onset of actionSubjective effects (energy, exercise tolerance) typically reported within 1–2 weeks of consistent dosing in research-community reports. Not validated in any human clinical study.

In depth

SLU-PP-332 is a synthetic small-molecule pan-agonist of the estrogen-related receptors α, β, and γ (the "ERR" family of orphan nuclear receptors). The compound was developed in the Burris laboratory (with Walker and Elgendy leading the medicinal chemistry) in the Saint Louis University / Washington University in St. Louis orbit — hence the SLU prefix — and was first characterized in published work in 2023.[¹][²] Its mechanism is direct activation of the ERR transcriptional pathway, which sits upstream of mitochondrial biogenesis, fatty acid oxidation, and the aerobic gene expression program activated during endurance exercise.

Mechanism in detail. ERRs are orphan nuclear receptors closely related to the estrogen receptors (with which they share ~70% sequence identity in the ligand-binding domain) but with distinct ligand specificity and physiological roles. Endogenous activators of ERRs are not well-characterized; the receptors are constitutively active to some degree and modulate transcription of genes encoding mitochondrial enzymes (electron transport chain components, fatty acid β-oxidation enzymes, ATP synthase subunits), oxidative slow-twitch muscle fiber proteins, and exercise-related metabolic genes. Pharmacological activation by SLU-PP-332 amplifies this baseline transcriptional activity. In mouse models, SLU-PP-332 administration produces:[¹] - Increased mitochondrial function and cellular respiration in skeletal muscle cell lines - Increased type IIa oxidative skeletal muscle fibers (the slow-twitch, fatigue-resistant phenotype) - Enhanced exercise endurance and exercise capacity - Increased energy expenditure and fatty acid oxidation - Reduced fat mass and improved glucose tolerance in obese mice

The "exercise mimetic" framing. SLU-PP-332's metabolic effects parallel some of the cellular and metabolic adaptations to endurance exercise — making the compound a candidate for "exercise mimetic" pharmacological intervention. The framing should be read directionally rather than literally: SLU-PP-332 activates many of the same intracellular pathways that exercise activates, but does not reproduce the cardiovascular adaptations, neurological effects, musculoskeletal loading, and broader physiological adaptations that actual exercise drives. Researchers using SLU-PP-332 on exercise-mimetic rationale should not interpret it as a substitute for actual training.

Oral bioavailability — a common misconception. SLU-PP-332 is widely sold and used as an oral preparation, but the published pharmacology does not support oral dosing. In a 2025 paper introducing the successor compound SLU-PP-915, the originating Burris lab wrote that SLU-PP-332 "improves aerobic performance in mice but lacks oral bioavailability" — SLU-PP-915 was designed specifically to be the orally active analogue.[⁴] The mouse studies underlying SLU-PP-332's exercise-mimetic data dosed the compound intraperitoneally, not orally. Researchers should keep two separate facts apart: that the research-chemical market supplies SLU-PP-332 in oral formats (true), and that the compound is orally bioavailable (not supported by the primary literature). No human pharmacokinetic study of any route exists.

Chemistry and structure-activity work. The originating group published the first comprehensive structure-activity relationship study of the SLU-PP-332 scaffold in 2026, optimizing the chemical series and mapping how ERR signaling responds to those modifications.[⁷] A 2026 systematic review of pharmacological ERRα/β/γ activation as an exercise mimetic concluded plainly that "clinical trials are needed to confirm their efficacy and safety in humans."[⁸]

Human-derived tissue — still not a human trial. One 2025 pilot study applied SLU-PP-332 to myoblasts isolated from human muscle biopsies in vitro, in the context of age-related muscle atrophy.[¹¹] This is ex-vivo work on human cells in a dish; the compound was never administered to a person. It does not constitute human clinical evidence, and the "no human trials" status is unchanged.

Common research interests. SLU-PP-332's research-community use spans: - Endurance / aerobic capacity enhancement — research-community use by athletes and active researchers on the rationale of supporting mitochondrial signaling and aerobic gene expression. - Metabolic / weight management — research-community use for fat mass reduction and improved glucose tolerance based on the obese-mouse data. - Longevity / "anti-aging" protocols — niche research-community use as a mitochondrial-support intervention; mechanistically aligned with AMPK/mitochondrial biogenesis pathways featured in longevity protocols. The nearest supporting evidence is a mouse study in which ERR agonism reversed mitochondrial dysfunction and inflammation in the aging kidney — an animal model, not a longevity outcome in people.[¹⁰] - Stack with MOTS-c, NAD+ precursors, or other mitochondrial-targeted compounds — research-community use in broader metabolic/mitochondrial protocols.

Regulatory status. SLU-PP-332 is sold as a research compound by research-chemical suppliers. No FDA-approved or pharmaceutical-grade product exists. The compound is not on the FDA 503A bulks list (which is specifically for peptide and biologic compounds compounded by 503A pharmacies — SLU-PP-332 is a small molecule and falls under different regulatory categories). Not named in the WADA 2026 Prohibited List as of the 2026 edition[³] — the metabolic-modulators class currently enumerates AMPK activators, PPARδ agonists, and Rev-erbα agonists, and ERR agonists are not among the named sub-classes. Not-named is not not-prohibited: WADA's S0 (Non-Approved Substances) prohibits at all times any pharmacological substance "with no current approval by any governmental regulatory health authority for human therapeutic use (e.g. drugs under pre-clinical or clinical development)", which describes this compound — so S0 captures it by default and it is off-limits in drug-tested sport. Verified against the local archive `docs/legal/wada-2026-prohibited-list.txt` (S0 clause + full-text search returning no hit) on 2026-09-07. That factual absence should not be read as reassurance. In 2026, two WADA-accredited laboratories published in-vitro metabolite and detection work on SLU-PP-332 explicitly for anti-doping purposes: the UCLA Olympic Analytical Laboratory characterized its metabolites, noting that "WADA prohibits the use of exercise mimetics and metabolic modulators in sports" and that identifying metabolites "is a critical step towards detecting its misuse,"[⁵] and the German Sport University Cologne laboratory characterized SLU-PP-332 and SLU-PP-915 as "novel pan-ERR agonists with doping potential," developing assays to "uncover the illicit use of these novel compounds."[⁶] SLU-PP-332 should therefore be treated as a high-risk, actively surveilled compound in the metabolic-modulator class. Researchers competing in WADA-tested sport should not assume it is permitted, and should confirm against the most recent annual Prohibited List edition and with their National Anti-Doping Organization before any competitive event.

Reported side effects

Commonly reported

  • Generally well-tolerated at the typical research-community doses
  • Mild GI symptoms (uncommon)
  • Increased subjective heat tolerance / sweating during exercise (reported in some research-community materials)
  • No consistent pattern of serious adverse events in research-community reports
  • The complete off-target profile in humans is uncharacterized given the absence of clinical trial data. ERRs are expressed across multiple tissues; pan-agonism could produce off-target effects not predicted from skeletal-muscle-focused preclinical work.
  • Effects on reproductive tissues — ERRs are expressed in reproductive tissues; pan-agonism's effects on reproductive function are not characterized.
  • Long-term safety in humans is essentially unknown. No multi-month human safety dataset exists.
  • Pregnancy and lactation safety — no data; default to contraindicated.

Contraindications and warnings

Pregnancy and lactation: no data; default to contraindicated

Pediatric use: no data — should not be used in researchers under 18

Active reproductive endocrine concerns — caution; ERRs are expressed in reproductive tissues

Active cardiac arrhythmia or unstable cardiovascular disease — caution; ERRγ is expressed in heart tissue and pan-ERR agonism is pharmacologically active there. Pan-ERR agonists have been studied in a mouse heart-failure model,[⁹] but the cardiac effects of these compounds in humans are uncharacterized

Regulatory note (US): SLU-PP-332 is sold as a research compound; not FDA-approved.

Regulatory note (WADA): SLU-PP-332 is not named in the 2026 WADA Prohibited List,[³] but it has no approval as a medicine anywhere, so WADA's S0 (Non-Approved Substances) category prohibits it by default, and two WADA-accredited laboratories have published detection assays for it in 2026 and describe it as having doping potential in the metabolic-modulator class.[⁵][⁶] Treat as high risk; do not assume it is permitted. Researchers competing in WADA-tested sport should confirm against the most recent edition and with their anti-doping organization.

Key terms

Small molecule
A low-molecular-weight chemical compound, distinct from peptides and proteins.
Oral
Taken by mouth, rather than injected.
Preclinical
Research done in cells or animals, before human clinical trials. Promising preclinical results don't always hold up in people.
Exercise mimetic
A compound that activates some of the same cellular pathways as exercise; the term is mechanistic and does not mean it replaces training.
Investigational
Still being studied and not yet approved by regulators for general use.

Sources

  1. Billon C, Schoepke E, Avdagic A, Chatterjee A, Butler AA, Elgendy B, Walker JK, Burris TP. (2024). A Synthetic ERR Agonist Alleviates Metabolic Syndrome. Journal of Pharmacology and Experimental Therapeutics, 388(2):232-240. doi: 10.1124/jpet.123.001733.(PMID 37739806)
  2. Billon C, Sitaula S, Banerjee S, Welch R, Elgendy B, Hegazy L, Oh TG, Kazantzis M, Chatterjee A, Chrivia J, Hayes ME, Xu W, Hamilton A, Huss JM, Zhang L, Walker JK, Downes M, Evans RM, Burris TP. (2023). Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity. ACS Chemical Biology, 18(4):756-771. doi: 10.1021/acschembio.2c00720.(PMID 36988910)
  3. World Anti-Doping Agency. The 2026 Prohibited List, International Standard (effective 1 January 2026). Canonical PDF: wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf. SLU-PP-332 is not listed in the 2026 WADA Prohibited List. S0 note (2026-09-07): not-named is confirmed, but this compound has no approval as a medicine anywhere, so WADA's S0 (Non-Approved Substances) captures it by default — the negative listing rules out a named prohibition, not prohibition.
  4. Billon C, Appourchaux K, Côté I, Burris TP. (2025). An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity. Journal of Pharmacology and Experimental Therapeutics, 393(1):103787.(PMID 41421047)
  5. Avliyakulov NK, Sobolevsky T, Ahrens E. (2026). Analysis and Identification of In Vitro Metabolites of Exercise Mimetic slu-pp-332 errα/β/γ Agonist for Doping-Control Purposes. Drug Testing and Analysis, 18(3):439-450.(PMID 41688415)
  6. Möller T, Krug O, Thevis M. (2026). In Vitro Metabolism and Analytical Characterization of SLU-PP-332 and SLU-PP-915: Novel Pan-ERR Agonists With Doping Potential. Rapid Communications in Mass Spectrometry, 40(8):e70039.(PMID 41588687)
  7. Okda HE, Zhao P, Hayes M, Duvall C, Quillin E, Fang H, Mohammed BM, Hegazy L, Burris TP, Elgendy B. (2026). Chemical optimization of the exercise mimetic SLU-PP-332 enables insight into estrogen-related receptor signaling. International Journal of Biological Macromolecules, 355:151450.(PMID 41850449)
  8. de Souza-Lima J, Astrosa-Martin BD, Galaz-Rodríguez CA, Silva-Bernal JE, Orellana-Pizarro LI, Mena-Díaz CA. (2026). [Pharmacological Activation of ERRα/β/γ as an Exercise Mimetic: Potential Therapeutic Applications]. Revista Médica de Chile, 154(2):237-245.(PMID 42024694)
  9. Xu W, et al. (2023). Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Oxidation and Mitochondrial Function. Circulation, 149(3):227-250.(PMID 37961903)
  10. Wang XX, et al. (2023). Estrogen-Related Receptor Agonism Reverses Mitochondrial Dysfunction and Inflammation in the Aging Kidney. The American Journal of Pathology, 193(12):1969-1987.(PMID 37717940)
  11. Bonanni R, et al. (2025). Targeting ERRs to counteract age-related muscle atrophy associated with physical inactivity: a pilot study. Frontiers in Physiology, 16:1616693.(PMID 40692696)

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Entry last updated 2026-09-03. Sourced from published literature and regulatory labelling; see Sources above.